Endobronchial adenosine monophosphate challenge causes tachykinin release in the human airway

Background

Adenosine 5 monophosphate (AMP) has been shown to cause bronchoconstriction and a sensation of chest tightness when inhaled by asthmatic subjects. This response is attenuated after repeated inhalation of bradykinin, suggesting that AMP may act in part by the release of neuropeptides.

Objective

This study examined neuropeptide release in the human airway after endobronchial AMP challenge.

Methods

Endobronchial AMP challenge was performed in 20 subjects and tachykinin levels were measured after endobronchial AMP challenge and after placebo endobronchial challenge with saline.

Results

All subjects coughed immediately after adenosine challenge. There was a significant increase in neurokinin A and substance P levels (P<.01, P<.01 respectively) when post-saline and post-AMP levels were compared. There was, however, no significant change in calcitonin gene related peptide levels (P=.37).

Conclusion

This study demonstrates that endobronchial AMP challenge causes tachykinin release in the human airway in vivo.

Key words: Tachykinin, neuropeptide, adenosine, endobronchial challenge

Abbreviations used: AMP, Adenosine 5′ monophosphate, CGRP, Calcitonin gene related peptide, NEP, Neutral endopeptidase, NKA, Neurokinin A, NKB, Neurokinin B, NPK, Neuropeptide K, PC₂₀ AMP, Provocative concentration of AMP causing a 20% fall in FEV₁, SP, Substance P